ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015
Hyperactivity of newborn Pten knock-out neurons results from increased excitatory synaptic drive.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
100 citing papers in PubMed, 136 citations in OpenAlex.
- Proteomics reveal PTEN as a critical mediator of sustained mitochondrial dysfunction during chronic spinal cord injury.Experimental neurology · 2026Article
- Analysis of PTEN Antagonistic Peptides (PAPs) in Neuronal Growth and Traumatic Brain Injury (TBI).Biomacromolecules · 2026Article
- A massively parallel CRISPR-based screening platform for modifiers of neuronal depolarization.Nature communications · 2026Article
- Targeted interneuron ablation in an mTORopathy model: Testing a two-hit mechanism of epileptogenesis.Progress in neurobiology · 2026Article
- Scaling of Neuronal Growth and Excitability Through Separable mTORC1 and mTORC2 Pathways.bioRxiv : the preprint server for biology · 2026Article
- PTEN Subcellular Localization Dictates Function.bioRxiv : the preprint server for biology · 2026Article
- PTEN regulates starburst amacrine cell dendrite morphology during development.Development (Cambridge, England) · 2026Article
- Mechanisms, translational opportunities for diabetic polyneuropathy.Frontiers in endocrinology · 2026Review
- G-Protein-Coupled Receptor-Microtubule Interactions Regulate Neurite Development and Protect Against β-Amyloid Neurotoxicity.Molecular neurobiology · 2025Article
- Autism Spectrum Disorder: The Cerebellum, Genes, and Pathways.Neurology international · 2025Review
- Research progress in glioma-related epilepsy (Review).Biomedical reports · 2025Article
- Article
- Seizures in brain tumors: pathogenesis, risk factors and management (Review).International journal of molecular medicine · 2025Review
- Convergent depression of activity-dependent bulk endocytosis in rodent models of autism spectrum disorder.Molecular autism · 2025Article
- Genetically encoded biosensor for fluorescence lifetime imaging of PTEN dynamics in the intact brain.Nature methods · 2025Article
- Article
- Developmental mechanisms underlying pediatric epilepsy.Frontiers in neurology · 2025Review
- PTEN in somatostatin neurons regulates fear and anxiety and is required for inhibitory synaptic connectivity within central amygdala.Frontiers in cellular neuroscience · 2025Article
- Mechanisms of brain overgrowth in autism spectrum disorder with macrocephaly.Frontiers in neuroscience · 2025Review
- PTEN deletion in the adult dentate gyrus induces epilepsy.Neurobiology of disease · 2024Article
40 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Developing neurons must regulate morphology, intrinsic excitability, and synaptogenesis to form neural circuits. When these processes go awry, disorders, including autism spectrum disorder (ASD) or epilepsy, may result. The phosphatase Pten is mutated in some patients having ASD and seizures, suggesting that its mutation disrupts neurological function in part through increasing neuronal activity. Supporting this idea, neuronal knock-out of Pten in mice can cause macrocephaly, behavioral changes similar to ASD, and seizures. However, the mechanisms through which excitability is enhanced following Pten depletion are unclear. Previous studies have separately shown that Pten-depleted neurons can drive seizures, receive elevated excitatory synaptic input, and have abnormal dendrites. We therefore tested the hypothesis that developing Pten-depleted neurons are hyperactive due to increased excitatory synaptogenesis using electrophysiology, calcium imaging, morphological analyses, and modeling. This was accomplished by coinjecting retroviruses to either "birthdate" or birthdate and knock-out Pten in granule neurons of the murine neonatal dentate gyrus. We found that Pten knock-out neurons, despite a rapid onset of hypertrophy, were more active in vivo. Pten knock-out neurons fired at more hyperpolarized membrane potentials, displayed greater peak spike rates, and were more sensitive to depolarizing synaptic input. The increased sensitivity of Pten knock-out neurons was due, in part, to a higher density of synapses located more proximal to the soma. We determined that increased synaptic drive was sufficient to drive hypertrophic Pten knock-out neurons beyond their altered action potential threshold. Thus, our work contributes a developmental mechanism for the increased activity of Pten-depleted neurons.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.